The anatomy, physiology, and pathologic processes that involve the spinal cord pose special concerns for the treatment of damaged or compromised spinal cord tissue. The preservation of both the three-dimensional structural anatomy and the microanatomical relationships of neurons (whose function depends on specific spatial relationships with other neurons and other supporting cells), as well as the maintenance of properly oxygenated blood flow and the homogeneous ground substance matrix in which the neurons survive, are vital to the survival and function of spinal cord tissues. Moreover, the inability of spinal cord cells to regenerate emphasizes the need to maximize survival of every possible neuron. For reasons such as these, treatment of both open and closed space pathology in the spinal cord poses special concerns.
Among the clinical problems that threaten survival of spinal cord tissue, the control of spinal cord edema, infection, and blood supply are central. The spinal cord responds to trauma and injury by collecting a significant amount of interstitial edema. Because the spinal cord is enclosed in a closed space (dura and the spinal canal), edema results in compression and compromise of the blood flow and nutritional performance of the spinal cord, which greatly impairs physiological recovery of the spinal cord and often of itself results in progression of compromise and death of the spinal cord. Currently available treatments for reducing edema include pharmacologic agents, such as glucocorticoids (Dexamethasone, Prednisone, Methyl Prednisolone), diuretics, and extensive surgical decompression. However, disadvantages to these treatments include irregular and unpredictable results, complications of the drugs, infection, and surgical complications.
The need for rapid and effective treatment is also vital due to the disastrous consequences and high likelihood of rapid propagation of infection and edema in the spinal cord. At present there are few successful methods available to treat pathologies affecting the intraspinal space, spinal cord parenchyma, and the surrounding structures. Where tissues elsewhere in the body can be treated with dressing changes, the spinal cord is not amenable to this type of treatment because of its precarious structure, propensity for infection, and potential for progression of injury. There is evidence that inflammation and immunological response to spinal cord trauma and other pathology are of equal or greater long term consequences than the initial trauma or insult. The response of the spinal cord to decreased blood flow secondary to edema results in hypoxia and ischemia/reperfusion-mediated injury. These injuries contribute to the neuropathological sequella, which greatly contribute to the adverse outcome of spinal injury.
In addition, the spinal cord requires a continuous supply of oxygenated blood to function and survive. Within a few minutes of complete interruption of blood flow to the spinal cord, irreversible spinal cord damage results. The spinal cord can, however, remain viable and recover from reduced blood flow for more prolonged periods. There is evidence that focal areas of the spinal cord can remain ischemic and relatively functionless for days and still recover. This finding has led to the concept of an ischemic zone, termed the penumbra or halo zone, that surrounds an area of irreversible injury. A secondary phenomena in the ischemic zone is the release of excitotoxins that are released locally by injured neurons, alterations in focal blood flow, and edema.
Vascular pathology of the spine may be a result of: inadequate blood flow to the spinal cord cells from decreased perfusion pressure, rupture of a blood vessel resulting in direct injury to the local spinal cord area, or by compression of adjacent tissue; intrinsic disease of the spinal cord blood vessels such as atherosclerosis, aneurysm, inflammation, etc.; or a remote thrombus that lodges in the spinal cord blood vessels from elsewhere such as the heart.
In cases of intraspinal hemorrhage, the hemorrhage usually begins as a small mass that grows in volume by pressure dissection and results in displacement and compression of adjacent spinal cord tissue. Edema in the adjacent compressed tissue around the hemorrhage may lead to a mass effect and a worsening of the clinical condition by compromising a larger area of spinal cord tissue. Edema in the adjacent spinal cord may cause progressive deterioration usually seen over 12 to 72 hours. The occurrence of edema in the week following the intraspinal hemorrhage often worsens the prognosis, particularly in the elderly. The tissue surrounding the hematoma is displaced and compressed but is not necessarily fatally compromised. Improvement can result as the hematoma is resorbed, adjacent edema decreased, and the involved tissue regains function.
Treatment of these conditions has been disappointing. Surgical decompression of the spinal cord can be helpful in some cases to prevent irreversible compression. Agents such as mannitol and some other osmotic agents can reduce intraspinal pressure caused by edema. Steroids are of uncertain value in these cases, and recently hyperbaric oxygen has been proposed.
Thus, though the application of negative (or sub-atmospheric) pressure therapy to wounded cutaneous and subcutaneous tissue demonstrates an increased rate of healing compared to traditional methods (as set forth in U.S. Pat. Nos. 5,645,081, 5,636,643, 7,198,046, and 7,216,651, as well as US Published Application Nos. 2003/0225347, 2004/0039391, and 2004/0122434, the contents of which are incorporated herein by reference), there remains a need for devices and methods specifically suited for use with the specialized tissues of the spinal cord.